The Role of Mitochondria in the Activation/Maintenance of SOCE: The Contribution of Mitochondrial Ca2+ Uptake, Mitochondrial Motility, and Location to Store-Operated Ca2+ Entry

2017 ◽  
pp. 297-319 ◽  
Author(s):  
Roland Malli ◽  
Wolfgang F. Graier
Keyword(s):  
Mitochondrial Motility

Intracellular motility of mitochondria: role of the inner compartment in migration and shape changes of mitochondria in XTH-cells

1978 ◽  
Vol 30 (1) ◽  
pp. 99-115
Author(s):  
J. Bereiter-Hahn
Keyword(s):  
Phase Contrast ◽  
Heart Cells ◽  
Underlying Principle ◽  
Good Accord ◽  
Contrast Microscopy ◽  
Mitochondrial Motility ◽  
Time Required ◽  
Shape Changes ◽  
Intracellular Motility

Mitochondrial movements have been followed by phase-contrast microscopy in living XTH-cells (Xenopus laevis tadpole-heart cells) in tissue culture. The same organelles have been viewed subsequently in electron micrographs. Locomotion of mitochondria proceeds at velocities up to 100 micrometer/min. Formation of branches of mitochondria and other shape changes may occur with the same speed. Mitochondrial motility can be classified into 4 types: (I) Alternating extension and contraction at the two ends of rod-shaped mitochondria. (2) Lateral branching. (3) Alternate stretching and contraction of arbitrary parts of a mitochondrion amounting to a kind of peristaltic action. (4) Transverse wave propagation along the organelle. Types I to 3 can be reduced to the same underlying principle; they cause locomotion. Formation of mitochondrial extensions is due to elongation of cristae. The observations are discussed in terms of 4 specific proposals. (I) Intracellular locomotion of mitochondria is caused by local enlargements and contractions of the organelles. (2) The shape changes are correlated with alterations in the arrangement of the cristae. (3) Such arrangements are not associated with overall swelling or shrinkage of the mitochondrion; they are local features. (4) Estimates of the time required for rearrangement of the inner compartment amount to less than 0.3 s for single crista arrangements during the fastest shape changes, and less than 1–3 s during slower alterations. This high velocity is in good accord with the hypothesis of energy conservation by conformational events during oxidative phosphorylation.

scholarly journals Role of Milton Domains in the Calcium-Dependent Regulation of Mitochondrial Motility

2010 ◽  
Vol 98 (3) ◽  
pp. 380a-381a
Author(s):  
Sudipto Das ◽  
Gyorgy Hajnoczky
Keyword(s):  
Calcium Dependent ◽  
Mitochondrial Motility

scholarly journals Role of Unc104/KIF1-related Motor Proteins in Mitochondrial Transport in Neurospora crassa

2005 ◽  
Vol 16 (1) ◽  
pp. 153-161 ◽  
Author(s):  
Florian Fuchs ◽  
Benedikt Westermann
Keyword(s):  
Neurospora Crassa ◽  
Mammalian Cells ◽  
Transport Systems ◽  
Eukaryotic Cells ◽  
Mitochondrial Transport ◽  
Specific Subgroup ◽  
Mitochondrial Motility

Eukaryotic cells use diverse cytoskeleton-dependent machineries to control inheritance and intracellular positioning of mitochondria. In particular, microtubules play a major role in mitochondrial motility in the filamentous fungus Neurospora crassa and in mammalian cells. We examined the role of two novel Unc104/KIF1-related members of the kinesin family, Nkin2 and Nkin3, in mitochondrial motility in Neurospora. The Nkin2 protein is required for mitochondrial interactions with microtubules in vitro. Mutant hyphae lacking Nkin2 show mitochondrial motility defects in vivo early after germination of conidiospores. Nkin3, a member of a unique fungal-specific subgroup of small Unc104/KIF1-related proteins, is not associated with mitochondria in wild-type cells. However, it is highly expressed and recruited to mitochondria in Δnkin-2 mutants. Mitochondria lacking Nkin2 require Nkin3 for binding to microtubules in vitro, and mitochondrial motility defects in Δnkin-2 mutants disappear with up-regulation of Nkin3 in vivo. We propose that mitochondrial transport is mediated by Nkin2 in Neurospora, and organelle motility defects in Δnkin-2 mutants are rescued by Nkin3. Apparently, a highly versatile complement of organelle motors allows the cell to efficiently respond to exogenous challenges, a process that might also account for the great variety of different mitochondrial transport systems that have evolved in eukaryotic cells.

scholarly journals Amyloid-beta oligomers induce Parkin-mediated mitophagy by reducing Miro1

2020 ◽  
Author(s):  
Min Kyoung Kam ◽  
Dong Gil Lee ◽  
Bokyung Kim ◽  
Jae-Won Huh ◽  
H.J. Lee ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Neuronal Cell ◽  
Time Lapse ◽  
Mitochondrial Fragmentation ◽  
Mitochondrial Quality Control ◽  
Cell Functions ◽  
Mitochondrial Motility ◽  
Ros Scavenger ◽  
Time Lapse Imaging

Alzheimer’s disease (AD) is a neurodegenerative disease associated with the accumulation of amyloid-beta oligomers (AβOs). Recent studies have demonstrated that mitochondria-specific autophagy (mitophagy) contributes to mitochondrial quality control by selectively eliminating the dysfunctional mitochondria. Mitochondria motility, which is regulated by Miro1, is also associated with neuronal cell functions. However, the role played by Miro1 in the mitophagy mechanism, especially relative to AβOs and neurodegenerative disorders, remains unknown. In this study, AβOs induced mitochondrial dysfunction, enhanced Parkin-mediated mitophagy, and reduced mitochondrial quantities in hippocampal neuronal cells (HT-22 cells). We demonstrated that AβO-induced mitochondrial fragmentation could be rescued to the elongated mitochondrial form and that mitophagy could be mitigated by the stable overexpression of Miro1 or by pretreatment with N-acetylcysteine (NAC)-a reactive oxygen species (ROS) scavenger-as assessed by immunocytochemistry. Moreover, using time-lapse imaging, under live cell-conditions, we verified that mitochondrial motility was rescued by the Miro1 overexpression. Finally, in HT-22 cells from amyloid precursor protein (APP)/presenilin 1 (PS1)/Tau triple-transgenic mice, we noted that the co-localization between mitochondria and LC3B puncta increased. Taken together, these results indicated that upregulated ROS, induced by AβO, increased the degree of mitophagy and decreased the Miro1 expression levels. In contrast, the Miro1 overexpression ameliorated AβO-mediated mitophagy and increased the mitochondrial motility. In AD model mice, AβOs induced mitophagy in the hippocampus. Thus, our results would improve our understanding of the role of mitophagy in AD toward facilitating the development of novel therapeutic agents for the treatment of AβO-mediated diseases.

scholarly journals Mitochondrial transfer from mesenchymal stem cells improves neuronal metabolism after oxidant injury in vitro: The role of Miro1

2020 ◽  
pp. 0271678X2092814 ◽  
Author(s):  
Nancy Tseng ◽  
Scott C Lambie ◽  
Christopher Q Huynh ◽  
Bridget Sanford ◽  
Manisha Patel ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Opposite Effect ◽  
Cell Contact ◽  
Oxidant Injury ◽  
Mitochondrial Transfer ◽  
Neuronal Metabolism ◽  
Affected Tissue ◽  
Mitochondrial Motility

Stroke-induced cerebral ischemia is a major cause of death and disability. The disruption of blood flow results in neuronal and glial cell death leading to brain injury. Reperfusion restores oxygen to the affected tissue, but can also cause damage through an enhanced oxidative stress and inflammatory response. This study examines mitochondrial transfer from MSC to neurons and the role it plays in neuronal preservation after oxidant injury. We observed the transfer of mitochondria from MSC to mouse neurons in vitro following hydrogen peroxide exposure. The observed transfer was dependent on cell-to-cell contact and led to increased neuronal survival and improved metabolism. A number of pro-inflammatory and mitochondrial motility genes were upregulated in neurons after hydrogen peroxide exposure. This included Miro1 and TNFAIP2, linking inflammation and mitochondrial transfer to oxidant injury. Increasing Miro1 expression in MSC improved the metabolic benefit of mitochondrial transfer after neuronal oxidant injury. Decreasing Miro1 expression had the opposite effect, decreasing the metabolic benefit of MSC co-culture. MSC transfer of mitochondria to oxidant-damaged neurons may help improve neuronal preservation and functional recovery after stroke.

Role of dactinomycin in the improved survival of children with Wilms' tumor

JAMA ◽  
1966 ◽  
Vol 195 (12) ◽  
pp. 1005-1009 ◽  
Author(s):  
D. J. Fernbach
Keyword(s):  
Wilms Tumor

Role of the allergist in diagnosis and management of patients with uveitis

JAMA ◽  
1966 ◽  
Vol 195 (3) ◽  
pp. 167-172 ◽  
Author(s):  
T. E. Van Metre
Keyword(s):  
Diagnosis And Management

The power of norms to sway fused group members

2018 ◽  
Vol 41 ◽  
Author(s):  
Winnifred R. Louis ◽  
Craig McGarty ◽  
Emma F. Thomas ◽  
Catherine E. Amiot ◽  
Fathali M. Moghaddam
Keyword(s):  
Evolutionary Anthropology ◽  
Normative Systems ◽  
Violent Extremism ◽  
Identity Fusion ◽  
Group Members

AbstractWhitehouse adapts insights from evolutionary anthropology to interpret extreme self-sacrifice through the concept of identity fusion. The model neglects the role of normative systems in shaping behaviors, especially in relation to violent extremism. In peaceful groups, increasing fusion will actually decrease extremism. Groups collectively appraise threats and opportunities, actively debate action options, and rarely choose violence toward self or others.

Elaborating the role of reflection and individual differences in the study of folk-economic beliefs

2018 ◽  
Vol 41 ◽  
Author(s):  
Kevin Arceneaux
Keyword(s):  
Decision Making ◽  
Individual Differences ◽  
Cognitive Processes ◽  
Evolutionary History ◽  
Behavioral Responses ◽  
History Of ◽  
Economic Beliefs

AbstractIntuitions guide decision-making, and looking to the evolutionary history of humans illuminates why some behavioral responses are more intuitive than others. Yet a place remains for cognitive processes to second-guess intuitive responses – that is, to be reflective – and individual differences abound in automatic, intuitive processing as well.

The role of affect in feelings of obligation

2020 ◽  
Vol 43 ◽  
Author(s):  
Stefen Beeler-Duden ◽  
Meltem Yucel ◽  
Amrisha Vaish
Keyword(s):  
Positive Emotions ◽  
The Creation ◽  
Sense Of Obligation

Abstract Tomasello offers a compelling account of the emergence of humans’ sense of obligation. We suggest that more needs to be said about the role of affect in the creation of obligations. We also argue that positive emotions such as gratitude evolved to encourage individuals to fulfill cooperative obligations without the negative quality that Tomasello proposes is inherent in obligations.

Sign in / Sign up

Export Citation Format

Share Document